Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection
Identifieur interne : 000375 ( Pmc/Checkpoint ); précédent : 000374; suivant : 000376Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection
Auteurs : Manuel G. Feria-Garz N [Colombie] ; María T. Rugeles [Colombie] ; Juan C. Hernandez [Colombie] ; Jorge A. Lujan [Colombie] ; Natalia A. Taborda [Colombie]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Background: HIV-1 induces an uncontrolled inflammatory response of several immune components, such as inflammasomes. These molecular complexes, associated with Toll-like receptor (TLR) activity, induce the maturation and release of IL-1β and IL-18 and eventually induce pyroptosis. It has been previously demonstrated that HIV induces inflammasome activation, which is significantly lower in the gastrointestinal tissue and blood from people living with HIV-1 with spontaneous control of viral replication. Therefore, immunomodulatory agents could be useful in improving HIV prognosis. Objective: To evaluate the potential inhibitory effect of sulfasalazine (SSZ) on inflammasomes and TLRs in peripheral blood mononuclear cells (PBMCs) from people living with HIV and healthy donors. Methods: PBMCs were obtained from 15 people living with HIV and 15 healthy donors. Cells were stimulated with agonists of TLRs and inflammasomes and subsequently treated with SSZ. The concentration of IL-1β and the relative expression of NLRP3, NLRC4, NLRP1, AIM2, ASC, Caspase-1, IL-1β, and IL-18 were quantified. Results: Cells treated with SSZ exhibited a decreased IL-1β production after inflammasome and TLR stimulation, as well as regulation of inflammasome-related genes, in both people with HIV and healthy individuals. The concentration of IL-1β was positively correlated with the CD4+ T-cell count and negatively with the viral load. Conclusion: Our results suggest that SSZ has an immunomodulatory effect on inflammasome and TLR activation that depends on the clinical HIV status.
Url:
DOI: 10.3390/ijms20184476
PubMed: 31514274
PubMed Central: 6770882
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Feria-Garz N</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-04476">Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010</wicri:regionArea><wicri:noRegion>UdeA. Medellín 050010</wicri:noRegion></affiliation></author><author><name sortKey="Rugeles, Maria T" sort="Rugeles, Maria T" uniqKey="Rugeles M" first="María T." last="Rugeles">María T. Rugeles</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-04476">Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010</wicri:regionArea><wicri:noRegion>UdeA. Medellín 050010</wicri:noRegion></affiliation></author><author><name sortKey="Hernandez, Juan C" sort="Hernandez, Juan C" uniqKey="Hernandez J" first="Juan C." last="Hernandez">Juan C. Hernandez</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-04476">Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010</wicri:regionArea><wicri:noRegion>UdeA. Medellín 050010</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijms-20-04476">Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín 050016, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín 050016</wicri:regionArea><wicri:noRegion>Medellín 050016</wicri:noRegion></affiliation></author><author><name sortKey="Lujan, Jorge A" sort="Lujan, Jorge A" uniqKey="Lujan J" first="Jorge A." last="Lujan">Jorge A. Lujan</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-04476">Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010</wicri:regionArea><wicri:noRegion>UdeA. Medellín 050010</wicri:noRegion></affiliation></author><author><name sortKey="Taborda, Natalia A" sort="Taborda, Natalia A" uniqKey="Taborda N" first="Natalia A." last="Taborda">Natalia A. Taborda</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-04476">Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010</wicri:regionArea><wicri:noRegion>UdeA. Medellín 050010</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af3-ijms-20-04476">Grupo de Investigaciones Biomédicas Uniremington, Programa de Medicina, Facultad de Ciencias de la Salud, Corporación Universitaria Remington, Medellín 050016, Colombia</nlm:aff><country xml:lang="fr">Colombie</country><wicri:regionArea>Grupo de Investigaciones Biomédicas Uniremington, Programa de Medicina, Facultad de Ciencias de la Salud, Corporación Universitaria Remington, Medellín 050016</wicri:regionArea><wicri:noRegion>Medellín 050016</wicri:noRegion></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Background: HIV-1 induces an uncontrolled inflammatory response of several immune components, such as inflammasomes. These molecular complexes, associated with Toll-like receptor (TLR) activity, induce the maturation and release of IL-1β and IL-18 and eventually induce pyroptosis. It has been previously demonstrated that HIV induces inflammasome activation, which is significantly lower in the gastrointestinal tissue and blood from people living with HIV-1 with spontaneous control of viral replication. Therefore, immunomodulatory agents could be useful in improving HIV prognosis. Objective: To evaluate the potential inhibitory effect of sulfasalazine (SSZ) on inflammasomes and TLRs in peripheral blood mononuclear cells (PBMCs) from people living with HIV and healthy donors. Methods: PBMCs were obtained from 15 people living with HIV and 15 healthy donors. Cells were stimulated with agonists of TLRs and inflammasomes and subsequently treated with SSZ. The concentration of IL-1β and the relative expression of NLRP3, NLRC4, NLRP1, AIM2, ASC, Caspase-1, IL-1β, and IL-18 were quantified. Results: Cells treated with SSZ exhibited a decreased IL-1β production after inflammasome and TLR stimulation, as well as regulation of inflammasome-related genes, in both people with HIV and healthy individuals. The concentration of IL-1β was positively correlated with the CD4+ T-cell count and negatively with the viral load. Conclusion: Our results suggest that SSZ has an immunomodulatory effect on inflammasome and TLR activation that depends on the clinical HIV status.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Lawrence, T" uniqKey="Lawrence T">T. Lawrence</name></author><author><name sortKey="Gilroy, D W" uniqKey="Gilroy D">D.W. Gilroy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Paiardini, M" uniqKey="Paiardini M">M. Paiardini</name></author><author><name sortKey="Muller Trutwin, M" uniqKey="Muller Trutwin M">M. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id><journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id><journal-id journal-id-type="publisher-id">ijms</journal-id><journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title></journal-title-group><issn pub-type="epub">1422-0067</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31514274</article-id><article-id pub-id-type="pmc">6770882</article-id><article-id pub-id-type="doi">10.3390/ijms20184476</article-id><article-id pub-id-type="publisher-id">ijms-20-04476</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Feria-Garzón</surname><given-names>Manuel G.</given-names></name><xref ref-type="aff" rid="af1-ijms-20-04476">1</xref></contrib><contrib contrib-type="author"><name><surname>Rugeles</surname><given-names>María T.</given-names></name><xref ref-type="aff" rid="af1-ijms-20-04476">1</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-9200-5698</contrib-id><name><surname>Hernandez</surname><given-names>Juan C.</given-names></name><xref ref-type="aff" rid="af1-ijms-20-04476">1</xref><xref ref-type="aff" rid="af2-ijms-20-04476">2</xref></contrib><contrib contrib-type="author"><name><surname>Lujan</surname><given-names>Jorge A.</given-names></name><xref ref-type="aff" rid="af1-ijms-20-04476">1</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0001-6085-855X</contrib-id><name><surname>Taborda</surname><given-names>Natalia A.</given-names></name><xref ref-type="aff" rid="af1-ijms-20-04476">1</xref><xref ref-type="aff" rid="af3-ijms-20-04476">3</xref><xref rid="c1-ijms-20-04476" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-ijms-20-04476"><label>1</label>Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia, UdeA. Medellín 050010, Colombia</aff><aff id="af2-ijms-20-04476"><label>2</label>Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín 050016, Colombia</aff><aff id="af3-ijms-20-04476"><label>3</label>Grupo de Investigaciones Biomédicas Uniremington, Programa de Medicina, Facultad de Ciencias de la Salud, Corporación Universitaria Remington, Medellín 050016, Colombia</aff><author-notes><corresp id="c1-ijms-20-04476"><label>*</label>Correspondence: <email>nataliataborda@gmail.com</email></corresp></author-notes><pub-date pub-type="epub"><day>11</day><month>9</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>9</month><year>2019</year></pub-date><volume>20</volume><issue>18</issue><elocation-id>4476</elocation-id><history><date date-type="received"><day>26</day><month>6</month><year>2019</year></date><date date-type="accepted"><day>06</day><month>9</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Background: HIV-1 induces an uncontrolled inflammatory response of several immune components, such as inflammasomes. These molecular complexes, associated with Toll-like receptor (TLR) activity, induce the maturation and release of IL-1β and IL-18 and eventually induce pyroptosis. It has been previously demonstrated that HIV induces inflammasome activation, which is significantly lower in the gastrointestinal tissue and blood from people living with HIV-1 with spontaneous control of viral replication. Therefore, immunomodulatory agents could be useful in improving HIV prognosis. Objective: To evaluate the potential inhibitory effect of sulfasalazine (SSZ) on inflammasomes and TLRs in peripheral blood mononuclear cells (PBMCs) from people living with HIV and healthy donors. Methods: PBMCs were obtained from 15 people living with HIV and 15 healthy donors. Cells were stimulated with agonists of TLRs and inflammasomes and subsequently treated with SSZ. The concentration of IL-1β and the relative expression of NLRP3, NLRC4, NLRP1, AIM2, ASC, Caspase-1, IL-1β, and IL-18 were quantified. Results: Cells treated with SSZ exhibited a decreased IL-1β production after inflammasome and TLR stimulation, as well as regulation of inflammasome-related genes, in both people with HIV and healthy individuals. The concentration of IL-1β was positively correlated with the CD4+ T-cell count and negatively with the viral load. Conclusion: Our results suggest that SSZ has an immunomodulatory effect on inflammasome and TLR activation that depends on the clinical HIV status.</p></abstract><kwd-group><kwd>inflammasomes</kwd><kwd>toll-like receptors</kwd><kwd>sulfasalazine</kwd><kwd>inflammation</kwd><kwd>HIV</kwd></kwd-group></article-meta></front><floats-group><fig id="ijms-20-04476-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>The release of IL-1β by peripheral blood mononuclear cells (PBMCs) in response to inflammasome agonists and sulfasalazine (SSZ)<bold>.</bold> The production of IL-1β by PBMCs from healthy donors (<bold>A</bold>) and people living with HIV (<bold>B</bold>), which were treated with inflammasome agonist in vitro (ATP 2 mM for NLRP3; Flagellin 500 ng/mL for NLRC4; poly(dA;dT) 50 μg/mL for AIM2; and MDP 0.1 μg/mL for NLRP1) in the presence of 1 mM SSZ during 4 h of incubation or 2 h for ATP-treated cells, was quantified by ELISA. Statistical comparison between groups was performed using a Wilcoxon matched-pairs signed rank one-tailed test with a confidence level of 95%. (+: presence, −: absence).</p></caption><graphic xlink:href="ijms-20-04476-g001"></graphic></fig><fig id="ijms-20-04476-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Expression of NLRP1, AIM2, and NLRP3 inflammasomes in peripheral blood mononuclear cells (PBMCs) in response to sulfasalazine (SSZ)<bold>.</bold> The expression of inflammasome-related gene was quantified in PBMCs from healthy donors and people living with HIV. The PBMCs were stimulated with inflammasome agonists (MDP 0.1 μg/mL, ATP 2 mM, and poly(dA;dT) 50 μg/mL) in the presence of 1 mM SSZ during 4 h of incubation or 2 h for ATP-treated cells. qPCR experiments are as indicated: mRNA NLRP1 (<bold>A</bold>), mRNA AIM2 (<bold>B</bold>), and mRNA NLRP3 (<bold>C</bold>). The β-actin gene was used as a constitutive gene to normalize the RNA content. Statistical comparison was performed using a Wilcoxon matched-pairs signed rank one-tailed test with a confidence level of 95%. Significant differences are indicated at the top of the figure (* <italic>p</italic> < 0.05) (** <italic>p</italic> < 0.01).</p></caption><graphic xlink:href="ijms-20-04476-g002"></graphic></fig><fig id="ijms-20-04476-f003" orientation="portrait" position="float"><label>Figure 3</label><caption><p>Expression of inflammasome-related genes in peripheral blood mononuclear cells (PBMCs) in response to sulfasalazine (SSZ). The expression of inflammasome-related gene was quantified by qPCR in the PBMCs from healthy and people living with HIV, which were stimulated with inflammasome agonists (ATP 2 mM for NLRP3; Flagellin 500 ng/mL for NLRC4; poly(dA;dT) 50 μg/mL for AIM2; and MDP 0.1 μg/mL for NLRP1) in the presence of SSZ 1 mM during 4 h of incubation or 2 h for ATP-treated cells. This figure shows mRNA caspase-1 in the context of NLRP1 (<bold>A</bold>), and mRNA ASC in the context of NLRP3 (<bold>B</bold>), AIM 2 (<bold>C</bold>) and NLRC4 (<bold>D</bold>). Expression of IL-1β in the context of NLRP3 (<bold>E</bold>), NLRC4 (<bold>F</bold>), AIM2 (<bold>G</bold>), and NLRP1 (<bold>H</bold>). Expression of mRNA IL-18 in the context of NLRP1 (<bold>I</bold>). The β-actin gene was used as a constitutive gene to normalize the RNA content. Statistical comparison was performed using a Wilcoxon matched- pairs signed rank one-tailed test with a confidence level of 95%. Significant differences are indicated at the top of the figure (* <italic>p</italic> < 0.05) (** <italic>p</italic> < 0.01).</p></caption><graphic xlink:href="ijms-20-04476-g003"></graphic></fig><fig id="ijms-20-04476-f004" orientation="portrait" position="float"><label>Figure 4</label><caption><p>IL-1β release by peripheral blood mononuclear cells (PBMCs) in response to TLRs agonists and sulfasalazine (SSZ). IL-1β production by PBMCs from healthy donors (<bold>A</bold>) and people living with HIV (<bold>B</bold>); these cells were treated in vitro with TLR agonist (LPS 100 ng/mL; poly(I:C) 1 μg/mL; R848 1 μg/mL; Pam<sub>2</sub>CSK<sub>4</sub> 40 ng/mL; and CpG-K16 4 μg/mL) in the presence of 1 mM SSZ during 18 h of incubation and were quantified by ELISA. Statistical comparison between groups was performed using a Wilcoxon matched-pairs signed rank one-tailed test with a confidence level of 95%. (+: presence, −: absence).</p></caption><graphic xlink:href="ijms-20-04476-g004"></graphic></fig><fig id="ijms-20-04476-f005" orientation="portrait" position="float"><label>Figure 5</label><caption><p>Correlation between IL-1β release in response to inflammasome agonists and sulfasalazine (SSZ) in term of the CD4+ T cells count or viral load. The effect of SSZ on IL-1β release through inflammasomes was determined in people living with HIV, on the basis of the CD4+ T cell count (<bold>A</bold>,<bold>B</bold>) and viral load (<bold>C</bold>,<bold>D</bold>). The correlations were estimated using Spearman’s rank correlation coefficients. The <italic>r</italic> and <italic>p</italic> values of the correlations are indicated at the top of each figure; a <italic>p</italic>-value of <0.05 was considered statistically significant. Black spots represent PBMCs treated only with inflammasome agonists. White spots represent PBMCs treated with inflammasome agonists and SSZ. Dashed-line indicates the correlation trend in the presence of SSZ. Continuous line indicates the correlation trend in the absence of SSZ.</p></caption><graphic xlink:href="ijms-20-04476-g005"></graphic></fig><table-wrap id="ijms-20-04476-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">ijms-20-04476-t001_Table 1</object-id><label>Table 1</label><caption><p>Demographic and clinical data.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1"></th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">People Living with HIV<break></break>(<italic>n</italic> = 15)</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Healthy Donors<break></break>(<italic>n</italic> = 15)</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1"><italic>p</italic>-Value</th></tr></thead><tbody><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Age in years, median (min-max)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">28 (18–51)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">29 (19–55)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">0.49117</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Sex, Male:Female</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">11:4</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">8:7</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">0.1498</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Time of diagnosis in months median (min-max)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">15 (1–85)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD4+ T cell count in the blood median (min-max)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">438 (316–840)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Plasma HIV viral load in RNA copies/mL median (min-max)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">16,660 (2500–140,400)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td></tr></tbody></table></table-wrap></floats-group></pmc><affiliations><list><country><li>Colombie</li></country></list><tree><country name="Colombie"><noRegion><name sortKey="Feria Garz N, Manuel G" sort="Feria Garz N, Manuel G" uniqKey="Feria Garz N M" first="Manuel G." last="Feria-Garz N">Manuel G. Feria-Garz N</name></noRegion><name sortKey="Hernandez, Juan C" sort="Hernandez, Juan C" uniqKey="Hernandez J" first="Juan C." last="Hernandez">Juan C. Hernandez</name><name sortKey="Hernandez, Juan C" sort="Hernandez, Juan C" uniqKey="Hernandez J" first="Juan C." last="Hernandez">Juan C. Hernandez</name><name sortKey="Lujan, Jorge A" sort="Lujan, Jorge A" uniqKey="Lujan J" first="Jorge A." last="Lujan">Jorge A. Lujan</name><name sortKey="Rugeles, Maria T" sort="Rugeles, Maria T" uniqKey="Rugeles M" first="María T." last="Rugeles">María T. Rugeles</name><name sortKey="Taborda, Natalia A" sort="Taborda, Natalia A" uniqKey="Taborda N" first="Natalia A." last="Taborda">Natalia A. Taborda</name><name sortKey="Taborda, Natalia A" sort="Taborda, Natalia A" uniqKey="Taborda N" first="Natalia A." last="Taborda">Natalia A. Taborda</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|area= ChloroquineV1
|flux= Pmc
|étape= Checkpoint
|type= RBID
|clé= PMC:6770882
|texte= Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Checkpoint/RBID.i -Sk "pubmed:31514274" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |